The main metabolites of cholesterol are the bile acids which make easier its elimination through the feces by forming micelles, as reported by Small D. M. in The bile acids--Chemistry, Physiology and Metabolism, Vol. 1 Nair P. P. and Kritchevsky D. Eds., Plenum Press, N.Y., 249-355, (1971). During the enterohepatic circulation, a process of conjugation takes place in the liver between glycine and taurine and the free bile acids are produced by cholesterol before their secretion into the ductus bilifer and the duodenum. The bile acids take part in the mechanism of absorption of fats and other lipids into the intestinal lumen by forming mixed micelles. The primary bile acids, cholic and chenodeoxycholic, are transformed by the enteric bacteria into secondary bile acids, respectively deoxycholic and lithocholic acid. Before this process, the bile acids conjugated with glycine and taurine are also partially deconjugated or hydrolyzed by the enteric bacterial flora. The chenodeoxycholic (CDCA) and ursodeoxycholic (UDCA) acids are widely used in the treatment of the cholesterol binary lithiasis as alternative to surgical operation, as reported by Thistle J. L. e Hofmann A. F. in New Engl. J. Med., 289, 655 (1973) and by Maton P. N. et al. in Lancet, 2, 1297 (1977). Other therapeutical applications reported in literature refer to the treatment of the hepatopathies, described by Poupon R. et al. in Lancet, 1, 834 (1987), of the gastritis from billiary reflux: described by Stefaniwsky A. B. et al. in Gastroenterology, 89, 1000 (1985) and of the cystic fibrosis. The chenodeoxycholic acid (CDCA) has been the first bile acid used in the therapy of the cholesterol billiary calculosis; it is still used notwithstanding its scarce tolerability because its chronic use causes many side effects like diarrhea and raising of the hepatic enzymes (transaminase) that limit its therapeutical use. This compound is very effective in inhibiting the hepatic synthesis of the cholesterol (HMGCoA reductase) so that a bile undersaturated of cholesterol is produced; moreover the high detergence of the CDCA makes easier the disintegration of the gall-stones into the bile in the form of a micellar solution. The CDCA, moderately toxic both at the intestinal and hepatic level, is metabolized into the organism to lithocholic acid, a highly hepatotoxic bile acid. The metabolism of the CDCA in man generally takes place by intestinal absorption through a passive mechanism, conjugation with glycine and taurine from the liver, biliary secretion in these chemical forms which subsequently are absorbed through a passive (glycoconjugate) and active (tauroconjugate and glycoconjugate) mechanism. Throughout this enterohepatic circulation the molecule is partly absorbed and partly eliminated in the feces. The CDCA's epimer known as ursodeoxyoholic acid (UDCA), which differs from the CDCA only because of the orientation of the hydroxyl in position 7 (from 7.alpha. to 7.beta.), has been introduced into therapeutic use in 1980 to obviate the side effects of the CDCA. This structural modification, apparently very small, indeed causes deep changes both in the chimico-physical and in the pharmacotoxicological properties. In particular the UDCA is a molecule much more hydrophilic and less detergent than the CDCA and also the other bile acids normally present in the human bile like the deoxycholic and the cholic acid. While the chronic administration of CDCA causes its enrichment in the bile equal to about 90% of the overall bile acids, the administration of the same dosage of UCDA causes an enrichment not greater than 50% of the overall bile acids. This fact can be attributed to various factors like the failure to inhibit the synthesis of the endogenous bile acids from cholesterol and the in complete intestinal absorption of this latter. More recent studies showed how the mechanism of action responsible for the dissolution of the gall-stones from the UDCA is different from that of the CDCA. The UDCA is able to dissolve the gall-stones by means of a selective reduction of the biliary secretion of cholesterol coupled with an intestinal malabsorption of the cholesterol itself. The UDCA is not so active as the CDCA in inhibiting the synthesis of the cholesterol and of the bile acids from the cholesterol. A bile enriched 50% of UDCA or of its conjugates with glycine and taurine makes a mesophase with the cholesterol and the phospholipids and the mechanism of dissolution of the cholesterol takes place not through micelles but through a system containing also liposomes made by biliary phospholipids. The pharmacokinetic of the UDCA is similar to that of CDCA: the drug is absorbed in the first step through a passive mechanism, transported to the liver from the portal system, conjugated with glycine and taurine and so secreted to be reabsorbed through an active mechanism in glycoconjugate and tauroconjugate form at the ileum level. Also the UDCA is partly 7-dehydroxylated producing lithocholic acid, but with a slower kinetic than that of CDCA. This fact, coupled with the lower absorption at the intestinal level, makes the UDCA a molecule much less toxic than the CDCA, innocuous also at dosages ten times higher than the therapeutic doses. For these reasons the UDCA has been proposed in the last years as new drug in the hepatic pathologies and has proved its effectiveness in the therapy of the primitive biliary cirrhosis and of some kinds of cholestatic hepatopathies. The therapeutic indication of the UDCA is therefore both for the dissolution of the gall-stones of cholesterol and for the treatment of hepatopathies. Lastly it has to be taken into account that the form that accumulates in the organism after chronic administration of UDCA is not the drug itself but its hepatic metabolites, i.e. its conjugate forms, GUDCA and TUDCA, that probably are the active principles. These conjugate forms undergo a process of deconjugation and of 7-dehydroxylation to lithocholic acid from the intestinal bacterial flora and therefore the UDCA in this way loses part of its therapeutic effectiveness and increases its toxicity. To get around these serious drawbacks, new steroid derivatives have been synthesized, having a structure correlated with that of the ursodeoxycholic, hyodeoxycholic and hydroholic acids, in which the acidic function in position 24 is substituted with an amide function stable to the degradation caused by the intestinal bacteria in comparison with the physiological amides containing glycine and taurine. The selection of the amides has been carried out so that the resulting molecules assume the chimico-physical and pharmacological activities necessary to get a good therapeutical effectiveness and a low toxicity. The structural changes introduced affect the chimico-physical properties of the derivatives making easier their absorption and secretion during the permanence in the enterohepatic circulation because the changes of ionization and hydrophobicity affect the transportation of these substances in the hepatobiliar system and in particular reduce the metabolic workload of the liver to conjugate the molecules and contemporaneously significantly reduce the intestinal process of 7-dehydroxylation to lithocholic acid The structural changes favourably affect also the pharmacological properties of these new amides by increasing their effect on the dissolution of the gall-stones from cholesterol and also by means of a choleretic effect in the cholestatic pathologies. Because of these reasons the derivatives of the bile acids object of the present invention can find useful therapeutical application in the treatment of many pathologies of the hepatic tract like the dissolution of the gall-stones from cholesterol, the pathologies coming from cholestasis, in particular the chronic cholestatic hepatitis, the primitive biliary cirrhosis and the juvenile hepatopathy from cystic fibrosis.